Upper GI 2 Flashcards
hiatal hernia - more common in who?
Most common abnormality found on upper GI x-ray
■ More common in older adults and women
2 types of hiatal hernia (hernias slide in pairs)
sliding and Paraesophageal or rolling
sliding hernia (the slide goes down)
slides into stomach when pt is lying down
Paraesophageal or rolling hernia
Fundus and greater curvature of stomach roll up through diaphragm, forming a pocket alongside the esophagus
Acute paraesophageal hernia is a (a cute para needs a paramedic)
medical emergency
hiatal hernia - causes (big)
Structural changes occur with aging
▪ Weakening of muscles in diaphragm ▪ Increased intraabdominal pressure
▪ Obesity
▪ Pregnancy
▪ Heavy lifting
hiatal hernia - symptoms (Hernia - H)
May be asymptomatic
▪ Symptoms include
▪ Heartburn
▪ After meal or when lying supine
▪ Dysphagia
hiatal hernia - complications
■ GERD
■ Esophagitis
■ Hemorrhage from erosion
■ Stenosis
■ Ulcerations of herniated portion
■ Strangulation of the hernia
■ Regurgitation with tracheal aspiration
■ Increased risk of respiratory problems
hiatal hernia - diagnostics (the only 2 you know)
Esophagogram (barium swallow) and endoscopy
hiatal hernia - management - conservative therapy (and what meds?)
ConservativeTherapy
▪ Lifestyle modifications
▪ Eliminate alcohol
▪ Elevate head of bed
▪ Smoking cessation
▪ Avoid lifting/straining
▪ Reduce weight, if appropriate
▪ Use antisecretory agents and antacids
esophageal diverticula (divert the zinc w/ traction and epinephrine)
Occur in 3 main areas
1. Zenker’s diverticulum
▪ Most common location
▪ Above the upper esophageal sphincter 2. Traction diverticulum
▪ Near esophageal midpoint 3. Epiphrenic diverticulum
▪ Above the LES
Esophageal Diverticula Clinical Manifestations (same a gerd)
■ Dysphagia
■ Regurgitation
■ Chronic cough
■ Aspiration
■ Weight loss
Esophageal Diverticula Complications (the MAP diverts up)
■ Malnutrition
■ Aspiration
■ Perforation
Esophageal Diverticula Diagnostic Studies (the same 2)
■ Endoscopy
■ Barium studies
Esophageal Diverticula Interprofessional Care (touch neck)
■ Applying pressure at a point on neck to empty pocket of food
■ Diet may need to be limited to foods that are blenderized
■ Treatment may be necessary if nutrition disrupted
■ Surgery
▪ Endoscopic or open approach (associated w/ morbitidy - usually older ppl)
▪ Most serious complication is esophageal perforation
Esophageal Strictures - over long or short time?
Usually develop over a long time
Esophageal Strictures - causes - most common? (Gerdie is #1 strict)
▪ GERD: most common cause
▪ Ingestion of strong acids or alkalis ▪ External beam radiation
▪ Surgical anastamosis
▪ Trauma
Esophageal Strictures - manifestations (DRW has strictures)
▪ Dysphagia
▪ Regurgitation
▪ Weight loss
Esophageal Strictures - treatment
▪ Dilated endoscopically ▪ Surgical excision
▪ Patient may have a temporary or a permanent gastrostomy (opening in stomach)
Achalasia (atcha is paralyzed)
▪ Rare, chronic disorder
▪ Exact cause is unknown
▪ Peristalsis is absent in lower 2/3 of esophagus
LES pressure ↑
Achalasia - manifestations (atcha can’t swallow w/ a lump in her throat)
▪ Dysphagia
▪ Most common symptom
▪ Liquids and solids
▪ Globus sensation (lump in throat)
▪ Substernal chest pain
▪ During/after a meal
Achalasia Diagnostic Studies
▪ Esophagogram (barium swallow)
▪ Manometric studies of lower esophagus
▪ Endoscopy
Achalasia - treatment - Endoscopic pneumatic dilation (atcha needs balloons)
▪ Outpatient procedure
▪ Dilation of LES using balloons of progressively larger diameters
▪ Repeat dilations are often required
Achalasia - Symptomatic relief (drink water with meals, back atcha)
▪ Semisoft diet ▪ Eating slowly
▪ Drinking with meals
▪ Sleeping with head of bed elevated
Esophageal Varices (varices is varacose) what is the cause?
Dilated, tortuous veins at the lower end of the esophagus caused by portal HTN
Esophageal Varices - Large varices are more likely to
bleed.
Ruptured esophageal varices are the
the most life- threatening complication of cirrhosis and considered a medical emergency.
Peptic Ulcer Disease
Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin
peptic ulcers can occur in (pepi is in the LSD)
▪ Lower esophagus
▪ Stomach
▪ Duodenum
▪ Margin of gastrojejunal anastomosis after surgical procedures
acute peptic ulcer - heal fast or slow?
▪ Superficial erosion
▪ Minimal inflammation
▪ Short duration: resolves quickly when cause is identified and removed
chronic peptic ulcer - how long? and are they common?
▪ Long duration
▪ Muscular wall erosion with formation of fibrous tissue
▪ Present continuously for many months or intermittently throughout person’s lifetime
▪ More common than acute erosions
peptic ulcers - patho
■ Develop only in presence of an acid environment
■ Excess HCl may not be necessary for ulcer development
■ Pepsinogen converts to pepsin in presence of HCl acid and at pH of 2 to 3
■ pH increases to 3.5 or more when
– Food or antacids neutralize the stomach acid
– Drugs block acid secretion
■ Back diffusion of HCl acid into gastric mucosa results in cellular destruction and inflammation
■ Histamine is released from damaged mucosa
■ Causes vasodilation, increased capillary permeability and further secretion of acid and pepsin
Destroyers of mucosal barrier: - Helicobacter pylori (helicopter is ur ease)
Helicobacter pylori (2/3 of world’s pop is infected)
▪ Major risk factor for PUD
▪ Produces enzyme urease
▪ Urease activates immune response
▪ Antibody production
▪ Release of inflammatory cytokines
▪ Leads to increased gastric secretions and causes damage
Destroyers of mucosal barrier: NSAIDs and aspirin
▪ Inhibit prostaglandin synthesis
▪ Increase gastric acid secretion
▪ Reduce integrity of the mucosal barrier
▪ Responsible for majority of non-H. pylori peptic ulcers
▪ NSAIDs in presence of H. pylori increase risk of PUD
Destroyers of mucosal barrier: steroids (steroids shrink)
▪ ↓ Rate of mucosal cell renewal
▪ ↓ Protective effects
Gastric Ulcers (gastric ulcers go everywhere in the stomach) and who gets them? (women stress)
■ Occur in any portion of stomach
■ Less common than duodenal ulcers
■ More prevalent in women
■ Peak incidence >50 years of age
■ More likely than duodenal ulcers to result in obstruction
gastric ulcers - risk factors (3 things) HMR (gassy hummer)
▪ H. pylori
▪ Medications
▪ Bile reflux
Duodenal Ulcers (duo is prevalent and young)
▪ Account for ~80% of all peptic ulcers
▪ Occur at any age and in anyone
▪ ↑ Between ages of 35 and 45 years
▪ H. pylori is found in 90% to 95% of patients
▪ Associated with increased HCl acid secretion
Duodenal Ulcers - Increased risk: (Dua and Zellwiger have ulcers at the door)
▪ COPD
▪ Cirrhosis of liver
▪ Chronic pancreatitis
▪ Hyperparathyroidism
▪ Chronic kidney disease
▪ Zollinger-Ellison syndrome
stress-Related Mucosal Disease (SRMD) (this surgery and trauma is stressing me)
■ Also called physiologic stress ulcer
■ Acute ulcers that develop after major physiologic insult
▪ Trauma or surgery
Gastric ulcers - manifestations- pain how long after meals?
▪ Pain generally high in epigastrium
▪ 1–2 hours after meals
▪ “Burning” or “gaseous”
▪ Food aggravates pain if ulcer has eroded through gastric mucosa
Duodenal ulcer - manifestations - pain how long after meals? (Dua is 25)
▪ Pain in midepigastric region beneath xiphoid process
▪ Back pain—if ulcer is located in posterior aspect
▪ 2–5 hours after meals
▪ “Burning” or “cramplike”
▪ Tendency to occur, then disappear, then occur again
Gastric ulcer - G
great pain
Duadenal ulcer - D
decrease pain
3 complications with ulcers (think if they rip off or block)
▪ Hemorrhage
▪ Perforation
▪ Gastric outlet obstruction
▪ All considered emergency situations
hemmorhage - does pain increase or decrease?
▪ Most common complication of PUD
▪ Dudoenal ulcers cause more UGIB (upper GI bleeds) episodes than gastric ulcers
▪ Clinical Manifestations:
▪ Changes in vital signs, ↑ in amount and redness of aspirate ▪ Signals massive upper GI bleeding
▪ ↑ Amount of blood in gastric contents
▪ ↓ Pain because blood neutralizes acidic gastric contents
Perforation
■ Occurs when ulcer penetrates serosal surface with spillage of contents into peritoneal cavity
manifestations of perforation - pain how quickly? and bowel sounds?
▪ Sudden, dramatic onset
▪ Initial phase (0–2 hours after perforation)
▪ Sudden, severe upper abdominal pain- quickly spreads throughout abdomen ▪ Pain radiates to back
▪ Rigid, boardlike abdominal muscles
▪ Shallow, rapid respirations
▪ Tachycardia, weak pulse
▪ Bowel sounds absent
▪ Nausea/vomiting
perforation treatment
▪ Immediate focus:
▪ Stop spillage of gastric or duodenal contents into peritoneal cavity
▪ Restore blood volume ▪ NG tube
▪ IVF
▪ pRBCs may be necessary
▪ ECG if patient has history of cardiac disease ▪ Broad-spectrum antibiotics
▪ Open or laparoscopic repair
Gastric Outlet Obstruction (Distal stomach and duodenum obstruction is the result…)
■ Acute and chronic PUD can result in gastric outlet obstruction
■ Distal stomach and duodenum obstruction is the result of: ▪ Edema
▪ Inflammation
▪ Pylorospasm and fibrous scar tissue formation
Gastric Outlet Obstruction - Clinical manifestations: (projectile vomiting at the outlet mall) and when is pain worse?
▪ Pain worsens toward end of day as stomach fills and dilates ▪ Relief obtained by belching or vomiting
▪ Vomiting is common, often projectile
Gastric Outlet Obstruction - treatment
▪ Decompress stomach via NGT
▪ Correct any existing fluid and electrolyte imbalances
▪ PPI or H2 receptor blocker if obstruction due to active ulcer ▪ Balloon dilation for pyloric obstruction
▪ Surgery may be needed to remove scar tissue
PUD - diagnostic studies
Endoscopy with biopsy
▪ Most often used as it allows for
direct viewing of mucosa
▪ Tissue specimens can be obtained to identify H. pylori and rule out stomach cancer
▪ Determine degree of ulcer healing after treatment
PUD - diagnostic studies - non-invasive (pugs have urea on their breath)
Noninvasive tests for H. pylori ▪ Urea breath test
▪ Can determine active infection
▪ Stool antigen test
▪ Serum or whole blood antibody tests
▪ Immunoglobin G (IgG)
▪ Will not distinguish between past and current infection
PUD - diagnostic studies - invasive
Invasive tests for H. pylori infection ▪ Endoscopic procedure
▪ Biopsy of stomach
▪ Rapid urease testing
PUD diagnostic - con’t
Barium contrast study
▪ Reserved for patient who cannot
undergo endoscopy
▪ Not accurate for shallow, superficial ulcers
▪ Used in diagnosis of gastric outlet obstruction
▪ Gastric analysis
▪ Analysis of gastric contents for
acidity and volume
▪ NG tube is inserted, and gastric contents are aspirated
▪ Contents analyzed for HCl acid
PUD - labs (pud needs liver tests)
Laboratory analysis ▪ CBC
▪ Liver enzyme studies
▪ Serum amylase determination ▪ Stool examination for blood
PUD treatment
▪ Adequate rest
▪ Drug therapy
▪ Smoking cessation
▪ Dietary modification
▪ Long-term follow-up care
goal of PUD treatment
▪ Reduce degree of gastric acidity
▪ Enhance mucosal defense mechanisms
PUD aftercare - how quickly does the pain subside?
▪ Generally treated in ambulatory care setting
▪ Pain disappears after 3–6 days
▪ Ulcer healing requires many weeks of therapy
▪ Endoscopic examination most accurate method to monitor healing
PUD drug therapy
▪ PPIs
▪ H2R blockers
▪ Antibiotics
▪ Antacids
▪ Anticholinergics
▪ Cytoprotective therapy
Antibiotic therapy to tx H. pylori: (pylori is tough)
▪ No single agent has been
effective in eliminating H. pylori
▪ Prescribed concurrently with a PPI for 14 days
Antacids - what do they do? (the opposite of what you think)
▪ Adjunct therapy for PUD
▪ Increase gastric pH by neutralizing HCl acid
Cytoprotective drug therapy - long or short term therapy?
Used for short-term treatment
▪ Protection for esophagus, stomach, and duodenum
Cytoprotective drug therapy ex (socrates and miso protect my stomach)
▪ Sucralfate
▪ Misoprostol
PUD - nutritional therapy (pugs eat anything)
■ No specific dietary modifications
■ Eat and drink foods and fluids that do not cause symptoms
■ Avoid alcohol use
PUD nursing management - stool?
■ PMHx
■ Medication
■ Heartburn
■ Weight loss
■ Black, tarry stools
■ Epigastric tenderness
■ Nausea and vomiting
■ Abnormal laboratory values
■ Acute pain
■ Ineffective health management
■ Nausea
PUD professional care
Vagotomy and Pyloroplasty
PUD - most common post op complications (pugs get down in the dumps w/ low blood sugar and reflux)
▪ Dumping syndrome
▪ Postprandial hypoglycemia
▪ Bile reflux gastritis
dumping syndrome - how many pts get it? and how long does it last?
Experienced by 20% of patients after PUD surgery. symptoms usually lasts less than 1 hour
dumping syndrome
see other slide
PUD - nutrition post op (pugs eat dry food, with low sugar after surgery)
▪ Small, dry feedings daily
▪ Low carbohydrates
▪ Restricted sugar with meals
▪ Moderate amounts of protein and fat
PUD - Pernicious anemia is a long-term complication
▪ After total or partial gastrectomy
▪ Due to loss of intrinsic factor (substance that helps vitamin B12 be absorbed)
▪ Patient will require cobalamin replacement therapy
PUD - geriatric considerations - what is the first symptom? (let’s be frank, it’s geriatric)
▪ ↑ Morbidity/mortality in older adults ▪ Concurrent health problems
▪ ↑ Use of NSAIDs
▪ First manifestation may be frank gastric bleeding or ↓ hematocrit ▪ Treatment similar to that for younger adults
▪ Emphasis placed on prevention
Gastritis
■ Inflammation of gastric mucosa
■ One of most common problems affecting the stomach
■ May be acute or chronic
■ Result of a breakdown in gastric mucosal barrier
■ Stomach tissue unprotected from autodigestion by HCl acid and pepsin
Gastritis - nsaids do what? (Prostie doesn’t like nsaids)
▪ Direct irritating effect on gastric mucosa
▪ NSAIDs, including aspirin and corticosteroids, inhibit
prostaglandin synthesis
gastritis - Stomach acid and pepsin can (basically just get through)
diffuse back into the mucosa resulting in: ▪ Tissue edema
▪ Disruption of capillary walls
▪ With loss of plasma into gastric lumen ▪ Possible hemorrhage
Risk factors for NSAID-induced gastritis (age and gender)
▪ Being female
▪ Being over age 60
▪ Hx of ulcer disease
▪ Anticoagulants, other NSAIDs, or ulcerogenic drugs
▪ Having a chronic debilitating disorder
▪ Diet
▪ ETOH
▪ Microorganisms
▪ H. pylori
▪ Important cause of chronic gastritis
▪ Promotes breakdown of gastric
mucosal barrier
▪ Bacterial, viral, and fungal infections
Autoimmune atrophic gastritis - affects what area of the stomach? (atrophy in my body is fun)
▪ Affects fundus and body of stomach
gastritis - risk factors con’t (vomiting?)
▪ Anatomic changes following surgical
procedures
▪ Prolonged vomiting
▪ Intense emotional responses
▪ CNS lesions
acute gastritis - clinical manifestations (think of acute sickness) and common with group?
■ Anorexia
■ Nausea
■ Vomiting
■ Epigastric tenderness
■ Feeling of fullness
■ Hemorrhage
▪ Common with alcohol abuse ▪ May be only symptom
Chronic Gastritis
Clinical Manifestations (same as acute)
▪ Symptoms are similar to those of acute gastritis
▪ Loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning
▪ Essential for absorption of cobalamin (vitamin B12)
Acute gastritis - Diagnosis most often based on (think who gets acute)
patient’s symptoms and history of drug or alcohol use
Chronic gastritis
▪ Diagnosis may be delayed or missed because of
nonspecific symptoms
gastritis - Endoscopic examination with biopsy - is it necessary?
▪ Necessary for definitive diagnosis
gastritis - Samples of what? (Gastritis gets every test)
Samples of breath, urine, serum, stool, and gastric tissue to determine H. pylori infection
gastritis - Radiologic studies
Radiologic (x-rays) studies not helpful
gastritis - CBC
▪ CBC
▪ Confirm presence of anemia from blood loss or lack of intrinsic factor
▪ Occult blood test
▪ Serum tests for antibody to parietal cells and intrinsic factor
▪ Tissue biopsy with cytologic examination ▪ Rule out gastric cancer
chronic gastritis - care (not helpful)
Focuses on evaluating and eliminating specific cause
UGIB - upper GI bleeding - Obvious bleeding
▪ Hematemesis (heman is fresh)
▪ Bloody vomitus
▪ Appears fresh, bright red blood or “coffee grounds”
UGIB - upper GI bleeding - Melena (it’s in the name)
▪ Black, tarry stools
▪ Caused by digestion of blood in GI tract ▪ Black appearance—due to iron
UGIB - upper GI bleeding - Occult bleeding
▪ Small amounts of blood in gastric secretions, vomitus, or stools ▪ Undetectable by appearance
▪ Detectable by guaiac test
Esophageal origin - bleeding
– Chronic esophagitis
– GERD
– Mucosa-irritating drugs
– Smoking
– Alcohol use
Stomach and duodenal origin - bleeding (think ulcers)
– Peptic ulcer disease
■ Bleeding ulcers account for 40% of cases of UGI bleeding
– Drugs
■ Aspirin, NSAIDs, corticosteroids
– Stress-related mucosal disease (SRMD) - common among who?
■ Also called physiologic stress ulcers
■ Most common in critically ill patients
– Severe burns, trauma, or major surgery
– Patients with coagulopathy on mechanical ventilation
upper GI bleed - diagnosis (you know if, and do you wash away the blood?)
Endoscopy
▪ Primary tool for diagnosing source of upper GI bleeding ▪ Before performing
▪ Lavage may be needed for clearer view
▪ NG or orogastric tube placed, and room-temperature water
or saline used
▪ Do not advance tube against resistance
▪ Stomach contents aspirated through a large-bore (Ewald) tube to remove clots
upper GI bleed - diagostics - angiography - used when? (angie is the last resort)
Angiography
▪ Used to diagnose only when endoscopy cannot be done ▪ Invasive procedure
▪ May not be appropriate for high-risk or unstable patient
▪ Catheter placed into left gastric or superior mesenteric artery until site of bleeding is discovered
Emergency Assessment and Management of UGIB - ▪ Immediate physical examination with focus on (think losing too much blood)!
BP
▪ Rate and character of pulse
▪ Peripheral perfusion with capillary refill ▪ Neurologic status
Emergency Assessment and Management of UGIB - how often to assess output? (emergency every hour)
Indwelling urinary catheter for assessment of hourly output
Emergency Assessment and Management of UGIB - tele
▪ Tele/CPO
▪ Central venous pressure line for assessment of fluid volume status ▪ Supplemental oxygen
Emergency Assessment and Management of UGIB - abdonminal exam
▪ Presence or absence of bowel sounds
▪ Tense, rigid, boardlike abdomen: may indicate perforation and peritonitis
Emergency Assessment and Management of UGIB - Type and amount of fluids infused are based on physical and laboratory findings (gi bleed is bore ing)
▪ 2 large bore IVs
▪ Isotonic crystalloid- Lactated Ringers ▪ Volume replacement
▪ Whole blood, packed red blood cells, fresh frozen plasma
GI bleed - Endoscopic hemostasis therapy
▪ First-line therapy of upper GI bleed
▪ Goal: to coagulate or thrombose the bleeding vessel
▪ Useful for gastritis, Mallory-Weiss tear, esophageal and gastric varices, bleeding peptic ulcers, and polyps
GI bleed - surgical therapy
▪ Indicated when bleeding continues
▪ Regardless of therapy provided
▪ Site of bleeding identified
GI bleed - surgery may be needed if how much blood loss?
May be necessary when
▪ Patient continues to bleed after rapid transfusion of up to 2000 mL whole blood
▪ Remains in shock after 24 hours
GI bleed - acute phase -what are drugs used for? (Just 2 things)
During acute phase, used to
▪ ↓Bleeding
▪ ↓ HCl acid secretion
▪ Neutralize HCl acid that is present
upper GI bleeding - injection therapy
with epinephrine during endoscopy for acute hemostasis
▪ For bleeding due to ulceration
▪ Produces tissue edema → pressure on bleeding source
upper GI bleed - Somatostatin (inhibits gi secretions)
▪ Used for upper GI bleeding
▪ Reduces blood flow to GI organs and acid secretion
▪ Given in IV boluses for 3–7 days after onset of bleeding
upper GI bleed - nursing management - Signs/symptoms of shock
▪ Low BP
▪ Rapid, weak pulse
▪ Increased thirst
▪ Cold, clammy skin
▪ Restlessness
ulcer perforation - lethal or not? and common where?
■ Most lethal complication
■ Common in large penetrating duodenal ulcers
■ Perforated gastric ulcers often located on lesser curvature of stomach
■ Mortality rate associated with perforation of gastric ulcers is higher
large perforations - surgery?
■ Large perforations need immediate surgical closure
■ Small perforations may spontaneously seal
themselves
perforation - how quickly will bacterial peritonitis occur?
▪ Bacterial peritonitis may occur within 6–12 hours
▪ Difficult to determine from symptoms alone if gastric or duodenal ulcer has perforated ▪ Manifestations of peritonitis are the same
PUD aftercare - how long after can you take Aspirin and nonselective NSAIDs?
▪ Aspirin and nonselective NSAIDs are discontinued for 4–6 weeks
▪ Patients receiving low dose aspirin may need long-term PPI treatment
antacids - how long to start working? With and without food
▪ Effects on empty stomach in 20–30 minutes
▪ If drugs taken after meals, effects may last 3–4 hours
antacids and sodium
▪ ↑ Sodium preparations: used cautiously in older patients and patients with ↑BP, heart failure, liver cirrhosis, or renal disease
▪ Magnesium preparations: not to be used in patients with renal failure
▪ Can enhance or decrease the absorption of some drugs
autoimmune atrophic gastritis - Associated with (and linked with what?) I can atrophy my cancer and h pylori
increased risk of gastric cancer
▪ May be linked to presence of H. pylori and development of autoimmune chronic gastritis`
atchalsia - symptoms (atcha has bad breath and can’t burp)
▪ Halitosis
▪ Inability to belch
▪ GERD
▪ Regurgitation
▪ Weight loss
gastric outlet obstruction - symptoms (can’t poop at the outlet mall)
▪ Constipation is a common complaint
▪ Dehydration
▪ Decreased dietary intake
▪ Anorexia
▪ Swelling in stomach and upper abdomen
